本院24例抗生素等药物致肾毒性损害的回顾性分析

目的观察抗生素等药物致肾毒性损害的临床表现及病理改变。方法对2008年10月至2011年10月我院收治的24例临床诊断为药物性肾损害并发肾功能不全的病历资料进行回顾性分析。结果本组导致肾损害的药物主要包括抗生素、非甾体类抗炎药、抗肿瘤药物、免疫抑制剂。本组24例肾损害患者发生急性肾功能衰竭18例,病理诊断显示急性肾小管坏死12例,急性间质性肾炎6例,治疗后15例愈合出院,3例转为慢性肾损害;6例发生慢性肾功能衰竭,病理诊断显示慢性间质性肾炎,死亡1例,余缓解后出院。结论应用肾毒性药物时要注意用药的剂量、疗程、患者的年龄及生理状态,内科并发症也是用药的重要考虑因素,应用肾毒性药物期间要注意监测患者的尿常规及肾功能变化,及早发现并干预病情发展。     

临床药师对药物性肾损害的干预

目的减少药物性损害的发生。方法分析药物性肾损害的表现及其与药物剂量的关系。结果药物性肾损害主要表现为急性肾小管坏死、急性间质性肾炎、慢性间质性肾炎、肾小球肾炎、血管性损害等。结论临床药师对肾损害药物加强干预,可预防药物性肾损害。     

药物性肾损害的分类及预防研究

<正>近年来,由于临床药物的广泛应用甚至滥用,药物所致的肾脏损害日益受到人们的重视。研究显示,药物性肾损害的发生率呈上升趋势,药物导致急性肾小管坏死(ATN)或急性间质性肾炎(AIN)的发生率高达18.3%。多种药物可损伤肾     

36例不明原因肾功能衰竭患者的病理类型分析

目的探讨不明原因肾功能衰竭患者经皮肾穿刺活检的病理类型。方法对符合条件的36例不明原因肾功能衰竭患者进行肾穿刺活检,行光镜、电镜、免疫荧光检查,观察穿刺肾组织肾小球个数、病理类型。结果肾组织标本合格率100%。病理类型前3位为Ig A肾病(38.9%),狼疮性肾炎(16.7%),新月体肾炎、增生硬化性肾炎、高血压肾损害及间质性肾炎(均为11.1%)。结论不明原因肾功能衰竭患者通过肾穿刺活检,可明确病理类型,及时给予合适治疗方案,从而延缓了慢性肾功能衰竭的进程。     

抗菌药所致急性肾损伤38例临床分析

目的:观察分析抗菌药物肾损伤,指导临床合理用药。方法:回顾性分析近10年来抗菌药肾损伤患者致病药物、临床特征、实验室检查、诊断、治疗及转归。结果:本组40岁以上患者28例,占73%,相关致病药物9种,临床表现急性间质性肾炎综合征,急性肾小管坏死,急进性肾炎综合征,肾病综合症征和慢性间质性肾炎综合征。32例临床治愈,6例转为慢性肾损伤。结论:停用致病药物和对于少数表现为急进性肾炎综合征,肾病综合征患者以甲泼尼龙、环磷酰胺冲击治疗为抢救肾脏的有效措施。药物性急性肾衰竭者给予透析治疗一般预后良好。部分病人可转为慢性肾损害。     

风湿病的肾脏改变

风湿病是一侵犯全身多系统的疾病,常累及肾脏引起肾小球肾炎、间质性。肾炎、肾内坏死性血管炎,并可发生急性与慢性肾功能衰竭。肾功能衰竭是这类患者死亡的重要原因之一。目前随着对风湿病研究的深入,其肾脏损害日益被人们重视。风湿病肾脏损害的主要机制主要有三点：免疫复合物在肾小球内沉积、细胞免疫介导的。肾小球损害、肾小管及间质的免疫损害。现将常见的风湿性疾病的肾损害总结如下。     

回顾性分析本院抗生素等药物致肾毒性28例

目的 回顾性分析抗生素等药物所致的肾损害.方法 对本院2005年1月至2008年12月所发生的药物所致肾损害,进行归类统计分析和评价.结果 导致肾损害、急性肾衰竭、急性肾功能不全、急性间质性肾炎、慢性肾炎、肾病综合症的药物,主要包括:抗生素(13/28),NSAIDs(6/28)、抗肿瘤药物(2/28),抗高血压药(4/28)、其他(3/28);全部病例人院后,治愈10例,好转11例;转为慢性3例,自动出院3例,死亡1例.结论 要做到合理用药,早期干预,预防药源性肾损害的发生.     

102例冠心苏合丸相关性肾损害不良反应分析

目的:分析冠心苏合丸引起肾损害的不良反应临床特点。方法:回顾研究102例因服用冠心苏合丸引起相关性肾损害不良反应患者的临床资料,分析冠心苏合丸致肾损害的临床特点、ADR表现、服药情况、治疗方法等。结果:102例患者中,女性76例,占74.51%;平均年龄为(66.42±10.31)岁;平均服用药物时间为(8.45±7.55)年;服用1~9年出现ADR的患者占61.76%;102例ADR程度分级均为严重,临床表现均不典型,病情呈隐匿性进展,均伴有贫血,贫血程度与肾功能减退程度不平行;67例肾图检查均出现双侧肾功能中重度受损;98例B超双肾体积缩小,严重受损,且大小不对称,结构不清呈弥漫性改变;25例肾脏病理活检以中重度慢性小管间质性肾炎为主。结论:患者肾功能受损情况与服用冠心苏合丸的时间长短、服用剂量不平行,个体差异较大;肾功能呈进行性损害,对出现贫血、肾功能损害及肾脏大小改变的患者应追问其服药史,以求尽快确诊救治。     

急性间质性肾炎21例的临床与病理

急性间质性肾炎（AIN）是由多种病因引起的突然发生的以肾间质炎症水肿、炎症细胞浸润、肾小管呈不同程度退行性变伴肾功能不全的临床综合征,表现为急性肾功能衰竭（ARF）、肾间质水肿和炎性细胞浸润,肾小球和肾血管多正常或轻度病变。为了提高对AIN的诊治水平,现对本院近年来肾活检确诊的21例急性间质性肾炎患者的病因、临床表现、肾脏病理改变进行分析报告如下。     

32例慢性肾功能衰竭患者肾活检的临床体会

目的探讨慢性肾功能衰竭患者经皮肾穿刺活检的临床与病理。方法对符合条件的32例慢性肾功能衰竭患者进行肾活检,行光镜、免疫荧光镜、部分行电镜检查,观察肾穿刺组织肾小球个数、病理类型、并发症。结果肾组织标本合格率100%。病理类型前三位为IgA肾病(40.6%),狼疮性肾炎(12.5%),新月体肾炎、Ⅱ期膜性肾病、恶性高血压肾损害及局灶节段性肾小球硬化(均为9.4%)。并发症以镜下血尿最常见,共30例(占93.8%),肾周小血肿6例(占18.8%)大血肿1例(占3.1%)。结论慢性肾功能衰竭通过肾穿刺活检,大部分患者得到更为及时、合理、个体化治疗,进一步改善了病情和预后,从而延缓了慢性肾功能衰竭的进程。若条件允许进行肾活检的慢性肾功能衰竭患者,及时进行肾活检仍是安全的,且具有十分重要的意义。     

Drug-induced nephrotoxicity. Aetiology, clinical features and management

There is a growing number of hospitalised patients who develop a drug-induced renal problem because increasing numbers of potent drugs have been added to the therapeutic arsenal in recent years. The 3 clinical syndromes that can be recognised in drug-induced nephropathy are acute renal failure, chronic interstitial nephritis and the nephrotic syndrome. The first can be caused by prerenal problems, acute interstitial nephritis, acute tubular necrosis and intratubular obstruction. The most important drugs that cause prerenal failure are NSAIDs, captopril and cyclosporin. NSAIDs inhibit the synthesis of prostaglandins, and consequently vasoconstriction of the afferent arteriole leads to lowering of the glomerular filtration rate (GFR); captopril blocks the formation of angiotensin II (which also leads to a lower GFR), and should be used with caution in patients with stenotic renal arteries; cyclosporin causes vasoconstriction of the afferent arteriole, which is probably mediated by the sympathetic system. Combinations of these drugs result in increased nephrotoxicity. The drugs most likely to cause acute interstitial nephritis are antibiotics and NSAIDs. Normally, signs of an allergic reaction are also present. Acute interstitial nephritis is usually self-limiting, but in some studies it is claimed that steroids may promote recovery. Four important causal agents of acute tubular necrosis are aminoglycosides, amphotericin B, radiocontrast agents and cyclosporin. Approximately half of the cases of drug-induced renal failure are related to the use of aminoglycosides: generally, 10 days after start of treatment a nonoliguric renal failure develops, with recovery after withdrawal of the drug in almost all cases. The aminoglycosides are particularly nephrotoxic when combined with other nephrotoxic drugs. 80% of amphotericin B-treated patients develop renal insufficiency, a percentage that increases as the cumulative dose exceeds 5g. It is because of its unique antifungal properties that there are still some indications for the use of this highly nephrotoxic drug; the high percentage of nephrotoxicity can probably be prevented in part by sodium loading. The nephrotoxicity of radiocontrast agents is largely dependent on renal function: from 0.6% in patients with normal renal function to 100% in patients with a serum creatinine above 400 mumol/L. Diabetes mellitus does not add greatly to the risk of radiocontrast nephrotoxicity. The nephrotoxicity of cyclosporin is dose-dependent and reversible, although there are some reports of irreversibility after long term use. Cyclosporin can also result in nephrotoxicity in combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)     

127例药物不良反应分析

目的:分析引起不良反应的药物临床表现及防治。方法:回顾性分析临床用药发生不良反应的情况。结果:127例不良反应中,心血管药物77例,占60.63％;其它为内分泌、激素药物22例,占17.32％;抗生素11例,占8.66％;抗癌药3例,占2.36%;其它14例,占11.02％。重症不良反应48例,占37.79％;死亡6例,占4.72％.结论:心血管药物可能引致较严重的不良反应。     

内科常用药物相关的急性肾衰竭

药源性急性肾衰竭（DARF）是指药物引起的以急性水、电解质紊乱和酸碱平衡失调及氮质血症为主要特征的一组临床综合征。DARF是一种常见的药源性疾病，约占肾实质性急性肾衰竭的19％～40％。其临床特点是在用药数日或数周内出现少尿或非少尿型ARF，部分患者可同时出现药疹、药物热、贫血、肝功能损害、神经系统损害等表现。DARF最常见的临床病理类型有急性肾小管坏死、急性间质性肾炎。DARF的发病机制主要为药物引起肾血流动力学改变导致肾灌注量减少、对肾小管细胞的毒性作用导致急性肾小管坏死、免疫反应导致急性间质性肾炎、药物结晶沉积导致管腔阻塞或免疫介导的肾小球肾炎等。DARF的相关危险因素包括药物的肾毒性作用、剂量、疗程，以及患者的机体状态如：高龄、血容量不足、糖尿病、既往肾损害或肾功能不全等。DARF的常见致病药物有抗生素、非甾体抗炎药、利尿剂及某些中药等。本文重点介绍内科常用的心血管系统药物、消化系统药物及抗病毒药导致DARF的临床特点及其防治。     

药物相关性急性肾损伤76例分析

目的分析药物导致的急性肾损伤(AKI)的临床特点。方法对76例药物引起急性肾损伤病人的用药种类、剂量、疗程、肾损伤的临床特点及其治疗转归等方面进行分析。结果 76例药物引起急性肾损伤患者,经停用肾损伤药物,并给予护肾、营养支持、激素、血液透析等治疗后,大部分患者临床症状消失,肾功能恢复正常。结论药物引起急性肾损伤,经积极治疗后可以恢复正常。     

Drug-induced renal disease.

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.     

雷公藤多苷联合百令胶囊治疗慢性肾小球肾炎的临床观察

目的:观察雷公藤多苷片联合百令胶囊治疗慢性肾小球肾炎的临床疗效。方法:将我院慢性肾小球肾炎患者90例随机均分为对照组和联合组,2组均口服雷公藤多苷片(20 mg,tid)及常规对症基础治疗,联合组加服百令胶囊,5粒,tid。2组均连续用药3个月。比较治疗前后2组血糖、尿蛋白、肾功能指标的变化。结果:治疗后联合组总有效率(91.1%)明显高于对照组(82.2%)(P<0.05)。联合组24 h尿蛋白质量、血肌酐(Scr)、血尿素氮(BUN)均明显降低,与对照组比较差异均有统计学意义(P<0.05)。联合组临床疗效总有效率明显高于对照组(P<0.05)。2组均未见明显不良反应。结论:雷公藤多苷联合百令胶囊治疗慢性肾小球肾炎疗效较好,不良反应较少。     

血液透析抢救药物中毒所致的急性肾功能衰竭56例

目的探讨血液透析对抢救急性药物中毒所致的急性肾衰的有效性.方法对56例药物中毒所致的急性肾衰患者的血透疗效进行分析.结果56例成功抢救5 3例,占94.64%,3例死亡,占5.37%.结论抢救药物中毒所致的急性肾衰的关键在于早期的预防性透析,以及处理好相应的并发症.     

Oxycodone involvement in drug abuse deaths. II. Evidence for toxic multiple drug-drug interactions

Recent surveys suggest that the abuse of drugs, often in combination, is pervasive throughout society. Adverse consequences of drug abuse tend to be attributed to the single drug "most likely" to be responsible. This is frequently seen in fatality cases, particularly those involving opioids. However, it is difficult to determine the specific cause of death when multiple drugs are involved. Although enhanced toxicity of alcohol and other centrally acting drugs with opioids has been well established in animal studies, there is a paucity of data in well-controlled human studies. We evaluated 1014 fatality cases involving oxycodone (OXC) for evidence of enhanced toxicity associated with multiple drug-drug interactions. We previously reported on these cases, and we classified them by a standardized method into groups that distinguished cases unrelated to drug abuse from those related to drug abuse, cases that involved only OXC from cases involving multiple drugs, drug-induced fatalities from drug-related fatalities, and cases in which the specific drug product OxyContin (oxycodone HCl controlled-release) tablets were identified from cases where OxyContin was not identified. Our working hypothesis was that OXC in combination with other centrally acting drugs is more toxic than OXC alone, evidenced by the finding of lower mean blood concentrations of OXC in multiple drug-induced deaths compared to single (OXC only) drug-induced deaths. Assessment of blood levels determined by specific assay methodology (primarily gas chromatography-mass spectrometry) in these cases provided the following mean postmortem concentrations of OXC: multiple drug-induced deaths, OxyContin identified, 0.93 mg/mL (N = 167); multiple drug-induced deaths, OxyContin not identified, 0.73 mg/mL (N = 579); single (OXC) drug-induced deaths, OxyContin identified, 1.55 mg/mL (N = 12); and single (OXC) drug-induced deaths, OxyContin not identified, 1.70 mg/mL (N = 15). Overall, mean OXC concentration trends were as follows: single (OXC), drug-induced, drug abuse deaths > multiple, drug-induced drug abuse deaths > drug-related drug abuse deaths approximately deaths unrelated to drug abuse; and deaths in which OxyContin was identified approximately deaths in which OxyContin was not identified, whether the deaths involved oxycodone alone or multiple drugs. Drug abuse patterns in the multiple drug-induced cases were complex. Over 135 drugs that were considered to be plausibly contributory to enhanced toxicity were identified in body fluids and tissues. Evaluation of mean OXC blood concentrations in cases that contained one, two, three, four, five, and six or more contributory drugs in combination demonstrated consistently lower mean OXC concentrations than those cases in which OXC was the only drug identified. A smaller number of cases were evaluated in the multiple drug-induced groups in which OXC was paired with a single other contributory drug. The overall mean OXC concentration for these cases was 0.71 mg/mL (N = 90) as compared to 1.64 mg/mL (N = 27) for the cases in the single drug-induced groups. The consistent finding of lower mean OXC blood levels associated with multiple drug-induced fatalities supports the stated hypothesis that OXC in combination with other centrally active drugs is more toxic than when OXC was the only drug involved. It was concluded that in cases of multiple drug fatalities, cause of death (COD) should not be attributed to any single drug. Rather, the unique combination of drugs, the pattern of drug use/abuse, and individual factors, such as tolerance to the respiratory depressant effects of opioids, must be taken into account in arriving at a valid COD statement.